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Abstract
Essence
Human cell DNA break repair pathway choice appears to vary with circadian timing through CRY1 control of DNA end resection.
Evidence
Mechanistic experiments in human cells tracked circadian DNA end resection and linked the oscillation to CRY1, CCAR2, CtIP, and DNA-PK phosphorylation.
Caveat
The cancer progression and radiation-therapy implications are not described with enough tumor-model or clinical detail in the abstract to infer treatment effects.
Simplified